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Title: Hypothalamus Stimulation Theory???? Post by Medlengough on Nov 1st, 2003, 1:40pm I've followed all the links posted here about the hypothalamus stimulation, but as yet have not read anything about the theory behind its' effectiveness. Does anyone already know the answer or seen a website or link concerning why they think the stimulation works? The best I've read is that it has to do with "interaction of neuronal activation". I'm wondering if the hypothesis is that the stimulation stops the abnormal production of a neuro pain modulator, such as Substance P or calcitonin, or does the stimulation restore the production of a normal neurotransmitter or hormone, such as epinephrine, acetylcholine, serotonin, etc. Thanks for any links, insight, or thoughts. Medlengough |
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Title: Re: Hypothalamus Stimulation Theory???? Post by Unsolved on Nov 1st, 2003, 3:57pm WOW...tough question. I was told that the stimulators keep the nerve pathways so busy that It cannot carry pain messages anymore. (I know it's not very technical but it's the best I could do for now) ;;D Unsolved |
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Title: Re: Hypothalamus Stimulation Theory???? Post by Mark C on Nov 6th, 2003, 3:43pm I agree...tough question. I found this included abstract. Given some time maybe I can fnd some more....very interesting subject. Dopamine and glutamate release in the nucleus accumbens and ventral tegmental area of rat following lateral hypothalamic self-stimulation Z. -B. You, , Y. -Q. Chen and R. A. Wise1 Center for Studies in Behavioural Neurobiology, Department of Psychology, Concordia University, Montreal, QC, Canada Received 27 April 2001; revised 10 July 2001; accepted 10 August 2001 Available online 20 November 2001. Abstract Rewarding hypothalamic brain stimulation is thought to depend on trans-synaptic activation of high-threshold (and thus rarely directly depolarized by rewarding stimulation) dopaminergic fibers of the medial forebrain bundle. We used in vivo microdialysis and high-performance liquid chromatography coupled with electrochemical or fluorometric detection to investigate the concurrent release of dopamine and glutamate in the nucleus accumbens septi and in the ventral tegmental area, as a function of lateral hypothalamic self-stimulation. Self-stimulation at a variety of stimulation frequencies and pulse widths increased levels of dopamine and its primary metabolites, dihydroxyphenylacetic acid and homovanillic acid in the nucleus accumbens. Lateral hypothalamic self-stimulation also induced significant increases in ventral tegmental area dopamine and metabolite levels, and the percentage increase of dopamine was higher in this region than in the nucleus accumbens. Local perfusion with the dopamine uptake inhibitor nomifensine (10 M) increased dopamine levels in the nucleus accumbens about three-fold and potentiated the increase of dopamine levels induced by self-stimulation. Nomifensine perfusion also induced a delayed decrease in nucleus accumbens glutamate levels, and self-stimulation did not modify this effect of the drug. Local perfusion with the D2-type dopamine receptor antagonist raclopride significantly increased both basal and self-stimulation induced dopamine release in the nucleus accumbens. Neither nomifensine nor raclopride perfusion significantly affected the maximal rates of self-stimulation. Perfusion with tetrodotoxin (2 M) into nucleus accumbens significantly decreased basal and prevented stimulation-induced increases in accumbens dopamine levels but only slightly decreased the rate of self-stimulation. In contrast, perfusion of tetrodotoxin (0.5 M) into the ventral tegmental area decreased basal and blocked stimulation-induced increases in both nucleus accumbens and ventral tegmental area dopamine levels; this treatment also blocked or strongly inhibited self-stimulation. While it had no effect on glutamate levels in the nucleus accumbens, lateral hypothalamic self-stimulation induced a significant and tetrodotoxin-sensitive increase in glutamate levels in the ventral tegmental area. Taken together, the present results indicate that, across a broad range of stimulation parameters, rewarding lateral hypothalamus stimulation causes major and persistent activation of the mesolimbic dopamine system, and suggest descending glutamatergic fibers in the medial forebrain bundle as a candidate for the directly activated descending pathway in lateral hypothalamus brain stimulation reward. I am not sure if this applies or not! PFDAN's Mark |
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Title: Re: Hypothalamus Stimulation Theory???? Post by floridian on Nov 6th, 2003, 5:08pm Here's a fairy tale that might be useful. Last century, evil scientists started destroying different parts of rats brains to see how it affected their behavior. Lesion this part, the rats go blind even though their eyes are fine. Lesion that part, and they will not bother to eat even when they are surrounded by food - to the point of starving to death. So the scientists rubbed their chins and concluded that all functions were fixed to specific parts of the brain. Enter a wacky scientist who was only semi-evil. For some unknown reason he destroyed the hunger center of a rat, then kept the rat alive via tube feeding. Eventually, the rat learned how to be hungry and eat. This really made the scientists rub their chins, as it shattered their idea that the brain is totally hard wired. They coined the term "recovery of function" to describe the adaptability of the brain. Apparently, any part of the brain could learn to do anything. Back to our own hypothalamic stimulators (and the 'pacemakers' used to help control parkinsons disease) . . . maybe they shake up the cells enough so that there is something like a recovery of function. - It wouldn't be a cross-region recovery, but an internal recovery. Maybe the cells were happy just watching TV, until the electric current shocked them into action, releasing neurotransmitters left and right. Maybe the cells were leaderless and despondent, and the pacemaker gets them talking to each other and organized into neighborhood councils. Neural networks have a self-organizing property to them that is impossible to fully explain, but neat to watch once you understand it. There is software based on the neural net idea that is not preprogrammed with a formula - it "learns" or is "trained" to solve a problem. These nets can be powerful, but even the best ones need an occasional kick to keep them from locking up. Somehow, the current stimulates real brain cells and keeps them from locking up. How? We're still working on that. Ok, maybe this fairy tale sucks. But hopefully its got you thinking about your brain. |
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Title: Re: Hypothalamus Stimulation Theory???? Post by Medlengough on Nov 8th, 2003, 5:03pm Thanks for the information and posts. Very interesting. I am to start a trial of Clomid today, but being female, may not have as good as results as the guys did. I'll post after my first trial of 5. My Doc thinks he can get me an appointment at MHNI, so I wanted to research all I could and understand as much as I can before I make the step. He also wants me to go out of state to have Genetic testing done. This will also take months to get an appointment and will be a big step. So for now I'll keep researching and try the Clomid. No one hopes this will help more than I do. Will let you know. Medlengough |
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Title: Re: Hypothalamus Stimulation Theory???? Post by floridian on Nov 9th, 2003, 3:41pm What genetic tests?? Is it related to CH, or something different? |
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Title: Re: Hypothalamus Stimulation Theory???? Post by Medlengough on Nov 10th, 2003, 10:40pm The Genetic testing is a Mitochondrial DNA test and a regular DNA test to rule out something called "Oculo Pharyngeal Dystrophy". Oddly, this rare conditon, (and not much is known about it yet except it has a genetic marker and is hereditary) has symptoms of unilateral eye pain that can be periodic or constant and is also associated with ptosis (drooping of the eyelid). I am not aware of a genetic marker for Cluster Headache, but sure wish there was. It would save alot of Neurologist visits. Maybe I am just unaware of such a test and maybe someone out there may have more information. My neurologist didn't mention one, but the main thing that sets me apart is that mine appears to definately be hereditary, involving both male and female ancestors. Alot of people's concensus is that Cluster headache doesn't appear to be hereditary. But that may be because it involves a recessive gene, which in my case became double recessive, due to centuries before of intermarriage due to religion. My one doc compares it to the Pharsee culture in India. The were very intelligent and tried to inbreed their genetic intelligence. Unfortunately, the passed along alot of double recessive pairs of genes that were not so good. My Doc also said it was possible that a particular gene mutated or became abnormal, only at a particular generation. In my case, it may have occured three generations ago. In other people's cases, it may just have mutated or gone haywire in their present generation. Thus they might feel that they didn't inherit it, but may pass it on in the future. They do a muscle biopsy for the mitochondrial DNA test, and he isn't sure they can do a good job in my area. I guess the tissue sample has to be handled very carefully. Has anyone else had any Genetic testing experience? Also does anyone have any advise about taking the Clomid, aside from protection? I don't know whether to take it morning, evening or night, but will watch out for blurred vision. Medlengough |
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Title: Re: Hypothalamus Stimulation Theory???? Post by Prense on Nov 10th, 2003, 11:06pm If I am not mistaken...in most cases a CH diagnosis is based on the info the patient gives the doc. Tests are performed to rule out ailments that can show up. |
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Title: Re: Hypothalamus Stimulation Theory???? Post by Cooked Brain on Nov 12th, 2003, 5:53pm here's some angels at work... [smiley=deal2.gif] http://www.aans.org/Library/Article.aspx?ArticleId=17571 |
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